and m~a MU~KGAARD ABSTRACT. Btiddal H, Thorsteinsson B, Munkgaard S. (Medical Departments E and B, Frederiksberg Hospital, Copenhagen, Denmark.) Long-term insulin-dependent diabetes mellitus with secondary pituitary insufficiency and regression of retinopathy. Acta Med Three women with insulin-dependent diabetes mellitus (IDDM) from childhood and early development of diabetic retidopathy are described. Insulin requirement was reduced to 5-12 IU daily in all three after relatively uncomplicated births and all had very brittle diabetes on this dosage. At re-examination 1622 years after these births and after 34-42 years of IDDM, regression of retinopathy was observed in two patients, while the third had a light retinopathy at the same level as initially. Other diabetic complications were few and none of the patients had nephropathy. Pituitary examination revealed incomplete hypopituitarism in all cases, human growth hormone (HGH) being the sole common factor lacking. These findings and a review of four similar cases reported previously lend some support to the hypothesis of HGH as a possible pathogenetic co-determinant in the development of diabetic retinopathy. Key words: diabetes mellitus, insulin, C-peptide, hypopituitarism, growth hormone, retinopathy. Sc-d 1983; 214: 225-9. The occurrence of spontaneous hypopituitarism in patients with insulin-dependent diabetes mellitus (IDDM) (the Houssay phenomenon) is well documented (1-3). However, only few cases with a sufficient period of observation after the onset of hypopituitarism and detailed examination of the pituitary function have been reported (4-8). Furthermore, late diabetic complications have only rarely been observed before the development of hypopituitarism, thus making observations of changes in the extent of these complications possible (4, 5, 8-10).This study describes three patients with long-term IDDM who developed partial pituitary insufficiency presumably due to Sheehan's syndrome, with emphasis on the investigation of the pituitary function, basal as well as stimulated, and the late diabetic complications.
PATIENTS AND METHODS
Hormone analysesSerum thyroxine (T4), triiodothyronine and thyrotropin (TSH) were measured by routine radioimmunoassay in our laboratory. Follicular stimulating hormone (FSH), luteinizing hormone (LH), growth hormone (GH) and prolactin (PRL) in serum were measured by radioimmunoassay. 17-Hydroxycorticoids (17-OHC), cortisol and 11-deoxy-cortisol in serum and urine were estimated by photometry in a commercial laboratory (Medicinsk Laboratorium, Copenhagen).Abbreviations: T4 = thyroxine, TSH = thyrotropin, TRH = TSH releasing hormone, FSH = follicular stimulating hormone, LH = luteinizing hormone, LHRH = LH releasing hormone, GH = growth hormone, PRL = prolactin, 17-OHC = 17-hydroxycorticoids, ACTH = adrenocorticotropic hormone, IDDM = insulin-dependent diabetes mellitus.
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